title: Infection of Helicobacter pylori in gastric adaptation to continued administration of aspirin in humans.
abstract: OBJECTIVE
  Involvement of Helicobacter pylori in aspirin-induced gastropathy and adaptation to aspirin remains unclear. The aim of this study was to compare gastric damage and adaptation after repeated exposures to acetylsalicylic acid in the same subjects before and after eradication of H. pylori.
  
  
  METHODS
  Before and after H. pylori eradication, 8 volunteers were given aspirin, 2 g/day during 14 days. Mucosal damage was evaluated by endoscopy and histological analysis of biopsy samples. Gastric microbleeding, DNA synthesis, prostaglandin E2 generation, and luminal contents of transforming growth factor alpha and its immunohistochemical expression were determined on days 0, 3, 7, and 14 of aspirin course.
  
  
  RESULTS
  In all subjects, aspirin-induced gastric damage that reached maximum on day 3. In H. pylori-positive subjects, this damage was maintained at a similar level up to day 14. After H. pylori eradication, the damage was significantly lessened both in endoscopy and histology at day 14 and accompanied by increased mucosal expression and luminal release of transforming growth factor alpha. Prostaglandin E2 generation was significantly greater in H. pylori-positive subjects than after H. pylori eradication, but aspirin treatment resulted in >90% reduction of this generation independent of H. pylori status.
  
  
  CONCLUSIONS
  Gastric adaptation to aspirin is impaired in H. pylori-positive subjects, but eradication of this bacterium restores this process.
authors.affiliation: Department of Medicine B, University of Münster, Germany. jan.konturek@uni-muenster.de
authors.forename: J W
authors.initials: JW
authors.lastname: Konturek
authors.forename: A
authors.initials: A
authors.lastname: Dembinski
authors.forename: S J
authors.initials: SJ
authors.lastname: Konturek
authors.forename: J
authors.initials: J
authors.lastname: Stachura
authors.forename: W
authors.initials: W
authors.lastname: Domschke
mesh_terms: D000222:Adaptation, Physiological; D000293:Adolescent; D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects* / Q000627:therapeutic use; D001241:Aspirin / Q000009:adverse effects* / Q000627:therapeutic use; D004247:DNA / Q000096:biosynthesis; D015232:Dinoprostone / Q000096:biosynthesis; D005260:Female; D005753:Gastric Mucosa / Q000098:blood supply / Q000187:drug effects* / Q000382:microbiology* / Q000473:pathology / Q000502:physiology; D006471:Gastrointestinal Hemorrhage / Q000139:chemically induced; D016481:Helicobacter Infections / Q000188:drug therapy / Q000503:physiopathology*; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D012313:RNA / Q000096:biosynthesis; D012039:Regional Blood Flow / Q000187:drug effects; D016211:Transforming Growth Factor alpha / Q000096:biosynthesis
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D016211:Transforming Growth Factor alpha; D012313:RNA; D004247:DNA; D015232:Dinoprostone; D001241:Aspirin